The relationship between peak aerobic fitness (peakVO2) and plasma leptin was assessed in 25 normal (BMI < 85th %tile) and 25 overweight (BMI > 85th %tile) youth, ages 7-17 years. In the overall analysis peakVO2 was related to leptin when expressed in mL/kg/min (R2 = .516, p < .0001), or as ml/kg(FFM)/min (R2 = .127, p = .01). The relationships between peak VO2 and leptin were no longer significant when percent bodyfat was added to the models. In subanalyses by weight groups, peak VO2: leptin relationships were not evident for normal weight, but remained for overweight youth. In conclusion the relationship between aerobic fitness and leptin in youth is dependent upon weight status.

Background

Obesity modifies inflammatory mediators, but little is known about how obesity modifies the inflammatory responses of exercising children. This study assessed the acute effect of exercise on inflammatory mediators in overweight children.

Methods

Twenty-eight overweight (OW) youth (body mass index > 85%) and 30 normal-weight (NW) controls of the same proportions of age and gender performed 10 2-minute bouts of cycle ergometry exercise above the anaerobic threshold, with 1-minute rest intervals between bouts. Pre- and postexercise blood samples were collected for white blood cell subpopulation and inflammatory cytokines.

Results

Baseline leukocyte populations were higher in OW youth (p < .05). Exercise increased most leukocyte subtypes for both groups (p < .05). Granulocytes remained elevated 2 hours postexercise (p < .05) for both groups, whereas monocytes remained elevated 2 hours postexercise for the OW children. Natural killer (NK) cells dropped below baseline 2 hours postexercise. Exercise significantly decreased CD4 and CD8 cells, which remained depressed 2 hours postexercise in the OW children. Baseline levels of interleukin (IL)-6 were congruent approximately 64% higher in OW children (p < .001). Exercise increased IL-6 in both groups (p < .001), which further increased 2 hours postexercise (p < .05). Tumor necrosis factor alpha, IL-1beta, and IL-1 receptor antagonist did not change with exercise.

Conclusions

Elevated baseline leukocyte subtypes and IL-6 levels in OW children suggest that childhood obesity is associated with a chronic low-grade inflammatory state. The acute inflammatory response to intense exercise appears to be similar between NW and OW children for most markers, but the depression of NK, CD4, and CD8 cells 2 hours postexercise suggests that an acute risk of mitogen-induced inflammation may exist in OW children after high-intensity exercise.

Obesity blunts catecholamine and growth hormone (GH) responses to exercise in adults, but the effect of obesity on these exercise-associated hormonal responses in children is unclear. Therefore, the aim of the present study was to asses the effect of childhood obesity on the counterregulatory hormonal response to acute exercise. Twenty-five obese children (Ob; body mass index > 95%), and 25 age, gender, and maturity-matched normal-weight controls (NW) participated in the study. Exercise consisted of ten 2-min bouts of constant-cycle ergometry above the anaerobic threshold, with 1-min rest intervals between each bout. Pre-, post-, and 120-min postexercise blood samples were collected for circulating components of the GH-IGF-I axis and catecholamines. There were no differences in peak exercise heart rate, serum lactate, and peak O2 uptake normalized to lean body mass between the groups. Obesity attenuated the GH response to exercise (8.9 +/- 1.1 vs. 3.4 +/- 0.7 ng/ml in NW and Ob participants, respectively; P < 0.02). No significant differences in the response to exercise were found for other components of the GH-IGF-I axis. Obesity attenuated the catecholamine response to exercise (epinephrine: 52.5 +/- 12.7 vs. 18.7 +/- 3.7 pg/ml, P < 0.02; norepinephrine: 479.5 +/- 109.9 vs. 218.0 +/- 26.0 pg/ml, P < 0.04; dopamine: 17.2 +/- 2.9 vs. 3.5 +/- 1.9 pg/ml, P < 0.006 in NW and Ob, respectively). Insulin levels were significantly higher in the obese children and dropped significantly after exercise in both groups. Despite the elevated insulin levels and the blunted counterregulatory response, none of the participants developed hypoglycemia. Childhood obesity was associated with attenuated GH and catecholamine response to acute exercise. These abnormalities were compensated for, so that exercise was not associated with hypoglycemia, despite increased insulin levels in obese children.